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Questions and Answers
What weight classification is considered a health risk?
What weight classification is considered a health risk?
Which factor is NOT a cause of obesity?
Which factor is NOT a cause of obesity?
Which of the following measurements is used to evaluate fat accumulation?
Which of the following measurements is used to evaluate fat accumulation?
What is the characteristic of life-long obesity?
What is the characteristic of life-long obesity?
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Which hormone plays a critical role in preventing the development of obesity?
Which hormone plays a critical role in preventing the development of obesity?
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What condition is associated with secondary obesity?
What condition is associated with secondary obesity?
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What is the Main differentiating factor between life-long and adult onset obesity?
What is the Main differentiating factor between life-long and adult onset obesity?
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Which of the following is an efferent signal generator in the regulation of energy balance?
Which of the following is an efferent signal generator in the regulation of energy balance?
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What role do POMC/CART neurons play in energy regulation?
What role do POMC/CART neurons play in energy regulation?
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Leptin primarily affects food intake by?
Leptin primarily affects food intake by?
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How do NPY/AgRP neurons affect energy balance?
How do NPY/AgRP neurons affect energy balance?
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Which of the following hormones is primarily responsible for increasing the basal metabolic rate?
Which of the following hormones is primarily responsible for increasing the basal metabolic rate?
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What effects does leptin have beyond regulating appetite?
What effects does leptin have beyond regulating appetite?
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What is the primary effect of adiponectin in the body?
What is the primary effect of adiponectin in the body?
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Which receptors are activated by NPY/AgRP neurons to promote weight gain?
Which receptors are activated by NPY/AgRP neurons to promote weight gain?
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What is one of the catabolic effects of leptin?
What is one of the catabolic effects of leptin?
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What is a major function of vitamin D?
What is a major function of vitamin D?
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What condition results from a lack of vitamin D in children?
What condition results from a lack of vitamin D in children?
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Which process primarily leads to the synthesis of vitamin D in humans?
Which process primarily leads to the synthesis of vitamin D in humans?
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What is a potential result of chronic toxicity related to retinoic acid?
What is a potential result of chronic toxicity related to retinoic acid?
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What synthesis process occurs in the liver regarding vitamin D?
What synthesis process occurs in the liver regarding vitamin D?
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What skeletal change can occur in children suffering from rickets?
What skeletal change can occur in children suffering from rickets?
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Which factor is NOT associated with vitamin D deficiency?
Which factor is NOT associated with vitamin D deficiency?
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What is the role of 1,25(OH)2D in relation to osteoblasts?
What is the role of 1,25(OH)2D in relation to osteoblasts?
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What is a typical clinical feature of Kwashiorkor?
What is a typical clinical feature of Kwashiorkor?
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Which of the following is NOT a common feature of Marasmus?
Which of the following is NOT a common feature of Marasmus?
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What differentiates cachexia from other forms of protein-energy malnutrition (PEM)?
What differentiates cachexia from other forms of protein-energy malnutrition (PEM)?
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Which factor contributes to the development of cardiac complications in anorexia nervosa?
Which factor contributes to the development of cardiac complications in anorexia nervosa?
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Which of the following describes the FLAG sign associated with Kwashiorkor?
Which of the following describes the FLAG sign associated with Kwashiorkor?
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What is a significant morphological change observed in Kwashiorkor?
What is a significant morphological change observed in Kwashiorkor?
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In bulimia nervosa, what is a major risk associated with frequent vomiting?
In bulimia nervosa, what is a major risk associated with frequent vomiting?
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Which of the following is a clinical feature of Marasmus?
Which of the following is a clinical feature of Marasmus?
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What hormonal change is associated with anorexia nervosa?
What hormonal change is associated with anorexia nervosa?
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What is a defining characteristic of obesity?
What is a defining characteristic of obesity?
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What is the primary characteristic of Harrisons sulcus?
What is the primary characteristic of Harrisons sulcus?
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What skeletal deformation occurs due to vitamin D deficiency in rickets?
What skeletal deformation occurs due to vitamin D deficiency in rickets?
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Which of the following skeletal changes is associated with vitamin C deficiency?
Which of the following skeletal changes is associated with vitamin C deficiency?
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What happens to the parietal bones during the nonambulatory stage of infancy when subjected to pressure?
What happens to the parietal bones during the nonambulatory stage of infancy when subjected to pressure?
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How does vitamin C deficiency primarily affect collagen synthesis?
How does vitamin C deficiency primarily affect collagen synthesis?
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What is a visible result of excessive osteoid due to vitamin D deficiency?
What is a visible result of excessive osteoid due to vitamin D deficiency?
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What nutritional deficiency is linked to the development of microcytic hypochromic anemia?
What nutritional deficiency is linked to the development of microcytic hypochromic anemia?
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Which process is disrupted in rickets, leading to skeletal deformation?
Which process is disrupted in rickets, leading to skeletal deformation?
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Study Notes
Nutritional Disorders
- Clinical features of Kwashiorkor:
- Occurs in children between 6 months and 3 years of age
- Growth failure
- Muscle wasting with preserved adipose tissue
- Edema (localized or generalized)
- Enlarged fatty liver
- Low serum proteins
- Anemia
- Alternating bands of light and dark hair - FLAG sign
- Clinical features of Marasmus:
- Common in infants under 1 year of age
- Growth failure
- Wasting of all tissues including muscles and adipose tissue
- No edema
- No hepatic enlargement
- Normal Serum proteins
- Anemia
- Monkey-like face, protuberant abdomen, thin limbs
- Morphology of Kwashiorkor:
- Enlarged fatty liver
- Atrophy of different tissues and organs
- Subcutaneous fat preserved
- Small bowel: mucosal atrophy & loss of villi and micro villi
- Bone marrow hypoplastic (plastic anemia)
- Cerebral atrophy
- Thymic & lymphoid atrophy
- Morphology of Marasmus:
- No fatty liver
- Atrophy of different tissues and organs including subcutaneous fat
- Rarely seen small bowel mucosal atrophy
- Hypoplastic heart
- Less marked cerebral atrophy
Secondary Protein Energy Malnutrition (PEM)
- Develops in chronically ill, older, and bedridden patients
- Obvious signs:
- Depletion of subcutaneous fat in arms, chest wall, shoulders or metacarpal regions
- Wasting of quadriceps and deltoid muscles
- Ankle or sacral edema
Cachexia
- PEM in patients with AIDS or advanced cancers
- Characterized by: extreme weight loss, fatigue, muscle atrophy, anemia, anorexia, and edema
- Exact cause unknown
- Mediators secreted by tumors contribute to cachexia:
- Proteolysis inducing factor
- Lipid-mobilizing factor
Anorexia Nervosa
- Self-induced starvation resulting in marked weight loss
- Similar to severe PEM
- Endocrine system effects:
- Amenorrhea (absence of menstruation due to decreased GnRH secretion)
- Symptoms of hypothyroidism
- Decreased bone density
- Dehydration and electrolyte abnormalities
- Major complication: Cardiac arrhythmias and sudden death due to hypokalemia (low blood potassium level)
Bulimia Nervosa
- Characterized by binge eating followed by induced vomiting
- More common than anorexia nervosa
- No specific signs or symptoms
- Diagnosis depends on psychological assessment
- Major complications due to frequent vomiting and chronic use of laxatives and diuretics:
- Electrolyte imbalance (hypokalemia) leading to cardiac arrhythmias
- Pulmonary aspiration of gastric contents
- Esophageal and gastric rupture
Obesity
- Defined as an accumulation of excess adipose tissue that imparts health risk
- A body weight of 20% excess over ideal weight for age, sex, and height is considered a health risk
- Etiology:
- Overeating
- Inactivity and sedentary lifestyle
- Genetic predisposition
- Loss of function mutation in leptin (hormone to maintain body weight)
- Mutation of melanocortin receptor 4 (MC4R) (regulation of food intake)
- Haploinsufficiency of BDNF (brain-derived neurotrophic factor) leading to obesity in WAGR syndrome (Wilms tumor, aniridia, genitourinary defects, mental retardation)
- Diets largely derived from carbohydrates and fats than protein-rich food
- Secondary obesity (hypothyroidism, Cushing's disease, insulinoma, hypothalamic disorders)
Measuring Fat Accumulation
- Body mass index (BMI: kg/m2):
- Normal BMI: 18.5 to 25
- Overweight: 25-30
- Obese: >30
- Skin fold measurements
- Various body circumferences, particularly the ratio of the waist-to-hip circumference
- Distribution of fat: central or visceral obesity is associated with more risk than excess accumulation of fat in subcutaneous tissue.
Types of Obesity
- Life-long obesity (hyperplastic obesity):
- Begins in childhood
- Characterized by an increased number of adipocytes on peripheral parts of the body
- Adult-onset obesity (hypertrophic obesity):
- Characterized by an increased size of fat cells and central obesity
- Fat accumulates on the trunk
Preventing Obesity
- Balance between calorie intake and expenditure
- Leptin plays a critical role in this regulation
- Neurohumoral mechanism regulating energy balance consists of three components:
- Peripheral (afferent) system:
- Generates signals from various sites
- Components:
- Leptin & adiponectin produced by fat cells
- Ghrelin from the stomach
- Peptide YY (PYY) from the ileum and colon
- Insulin from the pancreas
- Arcuate nucleus in the hypothalamus:
- Processes signals and generates efferent signals
- Consists of two subsets of first-order neurons:
- POMC/CART neurons:
- Enhance energy expenditure and weight loss
- Produce anorexigenic α-melanocyte-stimulating hormone (MSH)
- Activate melanocortin receptors 3 and 4 (MC3/4R) in second-order neurons
- Second-order neurons produce factors such as thyroid releasing hormone (TSH) & corticotropin releasing hormone (CRH) that increase basal metabolic rate and anabolic metabolism, thus favoring weight loss
- NPY/AgRP neurons:
- Promote food intake (orexigenic effect) and weight gain
- Activate Y1/5 receptors in secondary neurons
- Secondary neurons release factors such as melanin-concentrating hormone (MCH) and orexin, which stimulate appetite
- POMC/CART neurons:
- Efferent system:
- Two pathways: anabolic and catabolic pathways
- Controls food intake and energy expenditure respectively
- Peripheral (afferent) system:
Leptin
- Binds to leptin receptors in the hypothalamus, increasing energy consumption by:
- Stimulating POMC/CART neurons, which produce anorexigenic neuropeptides (MSH)
- Inhibiting NPY/AgRP neurons, which produce orexigenic neuropeptides
- Suppresses food intake and increases expenditure of calories
- Thermogenesis (controlled in part by hypothalamic signals that increase norepinephrine from sympathetic nerve endings in adipose tissue) is a catabolic effect mediated by leptin
- Additional functions: a proinflammatory cytokine, participating in the regulation of hematopoiesis and lymphopoiesis
Adiponectin
- Known as the "fat-burning molecule" and the "guardian angel against obesity"
- Directs fatty acids to muscle for oxidation
- Chronic toxicity is associated with weight loss, anorexia, nausea, vomiting, and bone and joint pain
Vitamin D
- Major function: maintenance of adequate plasma levels of calcium and phosphorus to support metabolic functions, bone mineralization, and neuromuscular transmission
- Key regulator of calcium and phosphate homeostasis
- Major source: endogenous synthesis from a precursor, 7-dehydrocholesterol, in a photochemical reaction that requires solar or artificial UV light in the range of 290 to 315 nm (UVB radiation)
- The reaction results in the synthesis of cholecalciferol, also known as Vitamin D3
- Produced in the skin from 7-dehydrocholesterol or ingested in the diet
- Converted in the liver into 25(OH)D and in the kidney into 1,25(OH)2D (1,25-dihydroxyvitamin D), the active form of the vitamin
- 1,25(OH)2D stimulates expression of RANKL (receptor activator of nuclear factor kappa beta (NFkB ligand)), an important regulator of osteoclast maturation and function, on osteoblasts, and enhances the intestinal absorption of calcium and phosphorus in the intestine
Vitamin D Deficiency
- Causes:
- Lack of dietary vitamin D
- Inadequate exposure to sunlight
- Intestinal malabsorption of fat
- Impaired hydroxylation due to hepatic and renal diseases
- Mechanism:
- Lack of vitamin D impairs the mineralization of the growing skeleton
- Signs of deficiency:
- Rickets (in children)
- Osteomalacia (in adults)
- Hypocalcemic tetany
Rickets: Skeletal Deformities
- Bow legs and lumbar lordosis
- Deformation of the chest results from the overgrowth of cartilage or osteoid tissue at the costochondral junction (producing the "rachitic rosary")
- Weakened metaphyseal areas of the ribs are subject to the pull of the respiratory muscles and bend inward (creating an anterior protrusion of the sternum; pigeon breast deformity)
- Harrison's sulcus (horizontal groove along the lower border of the thorax)
- Softened occipital bones may become flattened, and parietal bones can be buckled inward by pressure; with the release of the pressure, elastic recoil snaps the bones back into their original positions (craniotabes)
- An excess of osteoid produces frontal bossing (squared appearance to the head)
Rickets: Morphology
- Vitamin D deficiency results in an excess of unmineralized matrix in both rickets and osteomalacia
- The following sequence occurs:
- Overgrowth of epiphyseal cartilage due to inadequate provisional calcification and the failure of the cartilage cells to mature and disintegrate
- Persistence of distorted and irregular masses of cartilage that project into the marrow cavity
- Deposition of osteoid matrix on inadequately mineralized cartilaginous remnants
- Disruption of the orderly replacement of cartilage by osteoid matrix, with enlargement and lateral expansion of the osteochondral junction
- Abnormal overgrowth of capillaries and fibroblasts in the disorganized zone resulting from microfractures and stresses on the inadequately mineralized, weak, poorly formed bone
- Deformation of the skeleton due to the loss of structural rigidity of the developing bones
Vitamin C Deficiency
Causes
- Dietary lack of fresh fruits and vegetables
Mechanism
- Impaired collagen synthesis (Vitamin C is essential for collagen synthesis and cross-linking, which impacts tensile strength)
Clinical manifestations:
- Scurvy:
- Bone disease in growing children
- Hemorrhages and healing defects
- Vascular:
- Gingival bleeding
- Petechiae and ecchymoses
- Skeletal:
- Soft bones
- Growth retardation
- Delayed wound healing
Mineral Deficiencies
- Iron: Microcytic hypochromic anemia
- Iodine: Hypothyroidism, goiter, growth retardation
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Description
Explore the clinical features and morphological changes associated with Kwashiorkor and Marasmus. This quiz focuses on distinguishing between these two nutritional disorders, their symptoms, and implications for growth and development in children.
